1. Field of Invention
This invention relates to anterior cruciate ligament injury and repair.
2. Description of Prior Art
The anterior cruciate ligament (ACL) of the knee functions primarily to resist anterior translation of the tibia with respect to the femur. The ACL also contributes to rotational stability and resists hyperextension. In addition, the ACL has mechanoreceptors which provide proprioception—the conscious awareness of the limb position in space. The ACL may rupture from a variety of contact or noncontact injury mechanisms, especially when severe twisting occurs. The annual incidence of anterior cruciate ligament injuries in the United States is in excess of 100,000.
The ruptured ACL does not typically heal itself. Kurosaka, M., et al. (1998) J Bone Joint Surg 80, 1200-1203, reported spontaneous healing of ACL rupture in only two of fifty patients studied. Therefore, the current treatment for this injury is broadly divided into two approaches: activity modification and surgical reconstruction.
Activity modification requires that the patient accommodate to the injury by avoiding those maneuvers that would cause subluxation given absent ACL function. This is not a particularly rewarding strategy. To begin, activity modification demands giving up sports—often the very same activity that the patient was doing at the time of injury, and ostensibly enjoys. Furthermore, the natural history of the ACL-deficient knee is associated with meniscal tears, chondral damage, and degenerative changes. Irvine, G. B. and Glasgow, M. M. S. (1992) J Bone Joint Surg [Br] 74, 403-405 reported the incidence of major meniscal tears increases with time from the original ACL injury if untreated. They suggest the menisci undergo gradual attrition from abnormal loading and, in particular, increased shear. Indelicato, P. A. (1983) J Bone Joint Surg 65, 323-329 documented that chondral changes in ACL patients are more than twice as frequent in chronic patients who come to arthroscopy than in acute patients, implying that some of this damage was acquired after the injury.
Reconstruction of the ACL—i.e., replacement with a biological graft—as described in U.S. Pat. No. 5,139,520 Rosenberg is the current preferred surgical treatment for ACL rupture. This too is an imperfect solution; the problems encountered with reconstruction include graft site morbidity, inadequate graft to bone healing, and the loss of the proprioceptive function of the ACL. Kocher, M. S., et al. (2006) J Bone Joint Surg 84A, 1560-72, reported that on a discrete ordinal scale ranging from 1 to 10, which was framed by a score of 10 indicating “very satisfied”, a score between 5 and 6 indicating “neutral”, and a score of 1 indicating “very unsatisfied,” 15% of patients after ACL reconstruction (31 of 201 patients) had a patient satisfaction score of 5 or lower. Further, ACL reconstruction requires drilling about 10 mm tunnels in order for graft passage. These tunnels may alter the bony architecture which supports the joint surfaces and may cause premature closure of open growth plates in children.
Conspicuously missing from this short list of current treatment options is repair of the torn ligament. Surgeons shun ACL repair not because repair is impossible; suturing torn edges of tissue is a classic procedure and the existence of a Current Procedural Terminology (CPT) code for this operation, 27407, certainly testifies to the fact that people have tried. The reason that surgeons do not regularly perform this operation is simply that it does not work. The first primary repair of the ACL is attributed to A. W. Mayo Robson in 1895. Marshall, J. L., et al. (1979) Clin Orthop 143, 97-106 described a popular technique involving figure of 8 suture placement. While short-term results of repair were encouraging, Gollehon, D. L., et al. (1985) Orthop Clin North Am 16, 111-124, noted deterioration of these results over time.
The first problem with primary suture repair is technical. The ligament itself is short—measuring only about 33 mm—and is composed of longitudinal fibers. These features, in turn, make it difficult to place a stitch within the ligament and to retain such a stitch if placed, respectively. Ordinarily, when ligaments and tendons are repaired, the stitch is woven through a length of tissue, to have the suture circumferentially grasp the longitudinal fibers. With only 33 mm of tissue to work with, such an approach is not feasible.
Beyond the technical issues, the ACL is thought to have inherently poor healing potential, owing either to inadequate delivery and retention of healing factors from the circulation or to limited retention of these healing factors in the local milieu due to clot dissolution. It is our hypothesis—which serves as the basis of the invention herein described—that ACL repair fails because current methodology does not reestablish the correct and necessary biomechanical environment for healing, and that even if one were to surmount the difficulties in placing a secure stitch as well as delivering and retaining the healing factors, the repair is doomed to failure unless and until that correct and necessary biomechanical environment for healing is created and maintained. This proper environment comprises the maintenance of the native tibia-to-femur distance, full range of motion, and exposure of the ligament to some, but not excessive, mechanical loading.
The ACL is a critical component of the 4-bar cruciate mechanical linkage which dictates the spatial relationship between the femur and the tibia during flexion and extension of the knee. When the ACL is absent, tibiofemoral kinematics become grossly abnormal. Hsieh, Y., et al. (1998) Am J Sports Med 26, 201-209, demonstrated that excision of the ACL resulted in an increase in anterior laxity of the knee by a minimum of 5.5 mm at 0 degrees of flexion and a maximum of approximately 15 mm between 45 and 75 degrees of knee flexion. This distraction of the healing ACL results in failure to heal. Even if healing were to take place in the setting of distraction, the healed ligament would be longer than normal and functionally worthless. This underscores the point that the proper tibia-to-femur distance must be maintained.
Placing the knee in a cast can approximately maintain the correct tibia-to-femur distance and prevent distraction of the healing ACL, but the absence of knee motion deprives the healing graft of the mechanical signals it needs for proper maturation (so-called “ligamentization”—i.e., biological transformation into tissue resembling the native ligament). Moreover, immobilization leads to arthrofibrosis (stiffness of the joint) all too frequently. The stiff knee is certainly stable, but the resultant insult to normal range of motion leads to functional impairment in excess of what ligament deficiency itself would impose. Hence, this treatment is worse than the disease it attempts to heal. Further, soft tissue and padding interposed between the cast and the target bones limits precise maintenance of the appropriate distance.
We also note that stabilizing the knee with an extra-articular, indeed extra-corporeal, device, even if hinged, will not allow for maintenance of the precise tibia-to-femur distance. Bracing the knee has been employed as a method for approximating the femur and tibia in the setting of a torn ACL, but this approximation is inadequate to the task. For example, the four-point anterior cruciate ligament brace is described in U.S. Pat. No. 4,697,583 Mason, assigned to DonJoy Orthopedic, Inc. However, functional knee braces fail to completely reduce pathological translations and rotations due to the soft tissue interposed between the braces and the target bones. Ramsey D. K., et al. (2001) Clinical Biomechanics 16, 61-70 studied the skeletal kinematics of ACL deficient knees with and without the DonJoy Legend knee brace (Smith and Nephew DonJoy, Carlsbad, USA) and concluded that no consistent reductions in anterior tibial translations were observed as a function of the knee brace tested. Beynnon, B. D., et al. (2003) Am J Sports Med 31, 99-105, specifically found that bracing a knee with an ACL tear was not effective in reducing the abnormal anterior translations produced by the change between nonweightbearing and weightbearing postures.
A hinged external fixator capable of holding bony parts by means of screws or pins embedded in the bones was described in U.S. Pat. No. 4,696,293 Ciullo. This hinged external fixator can be used temporarily to rigidly control the relationship of the tibia with respect to the femur while allowing joint motion. However, Fitzpatrick, D. C., et al. (2005) Am J Sports Med 33, 1735-1741, reported that following the application of a hinged external fixator to a cruciate-deficient knee, anterior tibial translation with the knee at 30 degrees of flexion was 8.1 mm, compared to 4.5 mm in an intact knee. This pathologic anterior tibial translation is likely present because the true axis of rotation of the knee is not a fixed point—as a hinged device would impose—but rather one that migrates through the range of motion as described by Goodfellow, J. and O'Connor, J. (1978) J Bone Joint Surg 60B, 358-369. In addition, external fixators are all-too-frequently complicated by pin tract irritation, pin tract infection, osteomyelitis, fractured pins, and bony insertional pain. Velazquez, R. J., et al. (1993) J Bone Joint Surg 75A, 1148-1156, reported 17 pin tract infections for 61 uses of external fixators. Further, the pin tracts may interfere with tunnel placement if an ACL reconstruction is required in the future.
In sum, ACL repairs have failed because, inter alia, the correct biomechanical environment for healing—namely, maintaining the proper distance and tension between the femoral and tibial ACL attachment sites, throughout the full range of motion of the knee, at all times—has not been recreated by any of the methods disclosed in the prior art. The paradox of ACL repair is that the functions of an intact ACL are necessary to allow the repaired ligament to heal normally, yet if these functions were present, repair would not be needed. The instant invention provides a temporary, functional substitute for the injured ligament, allowing the repair to mature in the correct environment.